|COMMENTS ON PUBLISHED ARTICLE
|Year : 2018 | Volume
| Issue : 4 | Page : 324
The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension
Hilary P Grocott
Department of Anesthesia, Perioperative and Pain Medicine, University of Manitoba, Manitoba, Canada
|Date of Web Publication||11-Apr-2018|
Dr. Hilary P Grocott
Department of Anesthesia, University of Manitoba, CR3008 - 369 Tache Avenue, Winnipeg, Manitoba
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Grocott HP. The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension. Indian J Anaesth 2018;62:324
|How to cite this URL:|
Grocott HP. The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension. Indian J Anaesth [serial online] 2018 [cited 2020 Jun 4];62:324. Available from: http://www.ijaweb.org/text.asp?2018/62/4/324/229795
The recent retrospective study by Goyal et al. outlining the relationship between delayed graft function and pulmonary hypertension in patients undergoing renal transplantation addresses a number of potential responsible mechanisms for this relationship. For example, they suggest that haemodynamic instability (i.e. systemic hypotension) or deleterious circulating vasoactive substances can lead to poor perfusion and ischaemia of the transplanted kidney. Indeed, episodes of hypotension are not uncommon in the perioperative setting and patients with delayed graft functioning are also known to have higher levels of circulating endothelin-1, a potent vasoconstrictor that can lead to renal ischaemic injury, in addition to pulmonary hypertension itself.
However, an often under-recognised means by which kidney function can be impaired is through poor renal blood flow due to elevation in renal venous pressure that can result from pulmonary hypertension-associated right ventricular (RV) dysfunction. Elevations in the right atrial (RA) pressures can be reflected in the inferior vena cava and renal vein that can result in a reduction in overall renal perfusion pressure (i.e., arterial pressure–venous pressure). This likely explains the benefit to the acute treatment of RV dysfunction with pulmonary vasodilators and other inotropic agents that can reduce the RA pressure and improve renal function. Hence, although the circulating vasoactive substances that can lead to pulmonary hypertension could theoretically result in renal vasoconstriction, the main problem may not be the arterial flow to the kidney but rather the venous outflow from the kidney, which can similarly cause an ischaemic injury due to low transmural organ blood flow.
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| References|| |
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